Allergen avoidance underlies all other treatments of AR

There are several limitations to implementing allergen avoidance:

• Identification of allergens is necessary to successfully employ avoidance strategies

• Literature support for a clinically significant impact on symptoms from allergen avoidance, especially any single measure, is meager

• Quality of life may be negatively impacted by forced removal of a pet from the household

Outdoor plant pollen and mold/fungi parts:

• Limit outdoor exposure, especially during high pollen conditions (warm sunny days with wind and low humidity) and during mold/fungi spore release (shortly after rains)

• Wear a face mask during activities that disturb the earth and decaying vegetation

• Keep windows and doors closed

• Use air-conditioning when possible, but maintain clean equipment

Indoor allergens (house dust mite, mold/fungi, cockroaches, and pets):

• Use air-conditioning, as above

• Maintain humidity below 50% if possible, and maintain clean equipment

• Clean frequently and thoroughly to prevent mold growth (dilute bleach with detergent)

• Avoid exposed food and garbage to deter insects, especially in the kitchen

• Clean kitchen frequently and thoroughly

• Use roach traps that facilitate removal of allergen-containing bodies

• Vacuum frequently, and consider use of a high-efficiency particulate air (HEPA) filter

• Minimize carpeting, fabric covered furniture, and fabric wall/window coverings

• Cover bedding (pillow, mattresses, box springs) with allergen-proof, zippered cases

• Launder bedding frequently, in hot water (greater than 130°F or 60°C) if possible, to kill mite ova

• Consider acaricide (e.g., benzyl benzoate) treatment of carpets to kill mites and ova

• Put items that cannot be laundered (e.g., soft toys) in a plastic bag and freeze

• Keep pets out of bedroom and bath cats weekly, if possible Irritants:

• Avoid to the degree possible, all exposure to smoke, chlorine fumes, formaldehyde fumes, and other substances identified as irritant triggers in the patient (e.g., perfumes, newspaper ink)

The guideline document on AR published in August 2008 by the Joint Task Force (for AAAAI and ACAAI) includes an action plan (similar to what is used for asthma). The entire article, with the action plan, is available on the AAAAI website (http://www.aaaai.org/professionals/resources/pdf/rhinitis2008.pdf) in the public domain, for universal access.1 The application of the differently colored zones on the action plan is explained at the bottom of the form, which is on page S25 of the document. Many patients will benefit from having an action plan.

Table 62-4 Intranasal and Oral Medications for AR Corticosteroids

Intranasal a (budesonide, beclomethasone, ciclesonide, flunisolide, fluticasone [propionate and furoate], mometasone, triamcinolone) Oral (rarely used) Parenteral (not recommended) Antihistamines

Intranasal" (azelastine, olopatadine) Oralb

• First generation/sedating (cautious use in selected patients) (most OTC depending on strength: diphenhydramine, chlorpheniramine, clemastine, and others)

• Second generation/low- or nonsedating^ (desloratadine, fexofenadine, levocetir-izine; OTC: loratadine, cetirizine)

Mast cell stabilizer/cromone

Intranasal (OTC: cromolyn) Decongestant

Intranasal (short-term use) (tetrahydrozoline; OTC: phenylephrine, naphazoline, oxymetazoline) Oral b (OTC: phenylephrine; BTC c: pseudoephedrine) LTRA

Oral (montelukast is only one indicated)

Antimuscarinic

Intranasal (ipratropium)

Note: All products are Rx unless indicated OTC.

a First-line choices.

b Some products combine an antihistamine with a decongestant, sometimes with other ingredients.

c Behind the counter (OTC plus other requirements necessary; see the Decongestants section of text).

From Refs. 1-3, 24-28. First-Line Agents Corticosteroids

Corticosteroids are usually administered by the intranasal route for the treatment of AR. Occasionally, a short course of oral therapy (burst and taper) is necessary. This oral use of corticosteroids is best applied to overcome severe nasal congestion, particularly that due to rhinitis medicamentosa from intranasal decongestants (see Decongestant section below). Parenteral administration of corticosteroids in the management of AR is discouraged.1

Intranasal corticosteroids are considered the most effective therapy for AR. They are recommended as the drugs of choice for severe manifestations, and for those with moderate disease not controlled with oral and/or intranasal antihistamines. They provide very good relief for sneezing, itching, rhinorrhea, as well as nasal congestion and even ocular symptoms. Nasal congestion is often the most bothersome symptom of AR, and the most difficult to control. This is probably because it results from inflammation that predominates in the late phase of the allergic response in AR. Intranasal corticosteroids are the best agents for nasal congestion, probably because of their anti-inflammatory mechanism of action.1,13,21 Systemic corticosteroids (i.e., orally administered) are also effective, but they are used only as a last resort due to systemic side effects.

Several meta-analyses have evaluated the relative efficacy of intranasal corticosteroids in comparison with other types of pharmacologic therapy of AR. The majority (but not all) of the literature suggests that intranasal corticosteroids are superior to intranasal antihistamines, to oral antihistamines, even when combined with a leuko-

triene antagonist, and to a leukotriene antagonist alone. '

There are currently eight intranasal corticosteroid products available in the United States, including two different salt forms of fluticasone. Most (e.g., budesonide, ciclesonide, fluticasone furoate, mometasone, and triamcinolone) are usually given in a single daily dose. However, fluticasone propionate may be given either once or twice daily; beclomethasone is usually given twice daily; and flunisolide is given two or three times daily. Despite some differences in formulation, potency, chemistry, and pharmacokinetic and pharmacodynamic properties among the products, there is no good evidence that any single product is superior in efficacy. Intranasal corticosteroids are best given regularly, as the onset of action usually takes up to 12 hours and the maximum effects may be delayed up to 7 to 14 days.1, ,10 However, there is evidence that in some people the onset is within 3 to 4 hours, so these agents may even be used on an as needed basis.1,29 When nasal congestion is severe, intranasal administration may not be effective due to limited exposure to the nasal mucosa. In that situation, short-term intranasal decongestants may facilitate better exposure. See Table 62-5 for intranasal corticosteroid products.

The correct technique for administration of intranasal medication is important for optimum efficacy. Consult the individual product labeling for specific instructions. However, also see Table 62-6 for general instructions for the optimal administration of intranasal medications. The technique described maximizes exposure of the drug to the nasal mucosa to optimize efficacy, and minimizes both exposure to the nasal septum and loss of medication down the esophagus. See later for instructions about preparation and use of intranasal saline irrigations.

Most patients tolerate intranasal corticosteroids very well. Local side effects include nasal burning, irritation, and dryness, which may occur in up to 12% of pa-18 10 13 22

tients. ' ' ' ' Also, up to 1t% to 12% of patients may experience mild epistaxis.13,23 This may be partly due to the administration technique. Sore throat and head-

ache may be noted by some patients. Perforation of the nasal septum is a very rare side effect. This can be minimized by proper administration technique (see Table 62-6), specifically, directing the spray laterally (away) from the (medial) nasal septum.1,10

The older intranasal corticosteroids (beclomethasone, flunisolide, and budesonide)

have significant absorption, while the newer products (fluticasone, mometasone, and

ciclesonide) have bioavailability of no more than 1% to 2%. The decreased absorp tion minimizes systemic side effects. However, there is still some concern for growth suppression, other manifestations of hypothalamic-pituitary-adrenal (HPA) axis sup-

pression, bone, and ocular effects. Several studies have evaluated the effects of in-

tranasal and inhaled corticosteroids on HPA axis suppression and growth. ' Most have shown little or no clinically significant effects. The product most implicated with growth suppression is beclomethasone. One study demonstrated suppression in children using the drug for 1 year, but at twice the usual recommended dose.1 There is no confirmation of a causal effect of intranasal corticosteroids on posterior subcapsular cataracts, increased intraocular pressure, or decreased bone density; however, those with risk factors for any of these conditions should be monitored carefully for their development. Ultimately, patient preference for a specific intranasal corticosteroid may be determined more by cost and by formulation differences that affect odor and aftertaste.

Antihistamines

Antihistamines used for the treatment of AR are administered by either the oral or the intranasal route. These agents interact with the Hi (histamine type 1) receptor. Histamine is involved with both the early and the late phases of AR. Activation of Hi receptors in the nose, upper airway mucosa, and the eye produces the common manifestations of AR (sneezing, itching, rhinorrhea, nasal congestion, and ocular symptoms).

The antihistamines are very effective for the sneezing, itching, and rhinorrhea of AR. There is some effect to improve nasal congestion, but less so than for the other symptoms. There is also benefit for the ocular symptoms (e.g., itch, redness, tearing). Intranasal administration is more effective than oral administration for the nasal congestion, but less effective for the ocular symptoms. The onset of action by oral administration is usually within 1 to 2 hours, and that for intranasal administration within 30 18 13

minutes. ' ' All antihistamines probably provide better relief if used continuously (during symptomatic periods of seasonal AR, or for perennial or persistent AR), but they are also effective used only when needed.

Table 62-5 Intranasal Corticosteroids

Generic (Br»nd) ifimj

Usual Adult Dosage (Eiirh NoHril]

tJiii.il pediatric Doms* (E«h Noirrill

tehmtlUKCae (iipropiciiace

<12

6y(Jr>f IHQft» 1-2 ipijyi MMtLjSy

ffleconasieAQ)

32

i - spfdys ciocje <Jj|iy

t-ll yi CJ nvxt; 1-2 SfiiyiOiKi

Cktmonldo (Omnaris}

2 spays once daily

12 yo a more 2 iprayi once dally

Flunlsollde INasareO

JS

7 < |H jy*. two or ttiiee times daily

H yo or mow 1 ipray three limes dalty of

2 sprays Iwfco dally

J luckr.vky'H^ TLM LVLIL'

5fl

ispfiyiOftte daily

2-11 ye Of more 1 ^pr Ay once djily

F|u[kiW"«fWQfHanj|6i JFIonjH}

50

1-2 ipays once -da^y or 1 ipfif

4-11 a niote 1-2 iptays once ds^y

i*iciediily

MwrtcuwrK." (HdWiitii)

SO

2 iifldjfiOfKa daily

2-H yoijf moft 1 ipfjy w*e daily

Tfiairn Inolone aceionide

1-2 once dity

?-11 yo of mow 1 - J iprays once daily

ftdmoil AQ)

majuniao grams; yo, yerns old.

All pcoducluie FUA Pregnancy tateyofy £ ercepl ljudetonide, whili •■> B.

Table 62-6 Administration Instructions for Intranasal Medications majuniao grams; yo, yerns old.

All pcoducluie FUA Pregnancy tateyofy £ ercepl ljudetonide, whili •■> B.

Table 62-6 Administration Instructions for Intranasal Medications

1. Clear the nose of mucus and debris to the extent possible

2. Consult product labeling for preadministration instructions (e.g., shaking the container, priming the spray pump)

3. If seated or standing, do not just tilt head backward. This increases the amount of the dosage lost down the esophagus. This decreases efficacy and increases the potential for systemic absorption and thus systemic side effects

4. If standing, bend the head forward (flex the chin onto the chest) so that the nose is the lowest portion of the head. This is best for nasal sprays

If possible, lie in the prone position with the stomach (ventral side) on a flat surface or kneel down. Then, flex chin onto neck, so that the open nostrils are pointing as far upward, toward the ceiling as possible. This position may be best for nose drops (more volume than sprays)

An alternate position is to lie supine (on the back) on a flat surface, then bend the head backward (extend the head), again, so that the open nostrils point upward toward the ceiling

5. Use the contralateral hand to insert the spray nozzle or dropper into one nostril (i.e., the left hand for right nostril)

6. Use the other hand to occlude the opposite nostril (the one not being medicated)

7. Aim the spray or drops toward the outer (lateral) internal surface of each nostril, and away from the nasal septum (which is the inner or medial surface)

8. Breath in slowly but deeply through the medicated nostril

9. Repeat this procedure to apply medication to the other nostril

10. Consult the product labeling for cleaning instructions

11. See the text for information about preparation and use of saline irrigation

Antihistamine drugs used for AR are technically inverse agonists, not competitive

101321

antagonists; however, there may be little clinical significance to the difference. ' ' These drugs bind to the H1 receptor, changing its three-dimensional conformation such that it is kept in t he inactive state. This results in downregulation of H1 receptor activity and a decrease in end organ effects. These agents do not prevent release of histamine.

The oral agents are divided into first- and second-generation drugs. The first-generation agents are distributed among six chemical classes, including the more sedating ethanolamine class (e.g., diphenhydramine) and the least sedating alkylamine class (e.g., chlorpheniramine). Most sources now discourage the routine use of the first-generation agents for AR. This is due to their CNS and anticholinergic side effects. The CNS effects are primarily sedation, as well as impairment of cognitive function and performance of tasks. Studies have shown that decision making and driving or work performance are impaired even when the patient is unaware of any overt effects.1 There is also evidence of decreased performance at school and impaired learning, among pediatric patients.1 Some controversy remains, however, about how

common these problems truly are. The major anticholinergic (perhaps more accurately stated as antimuscarinic) effects include blurred vision, dry mouth, urinary retention, and constipation. The only possible advantage of the antimuscarinic properties is an additional effect to decrease rhinorrhea. However, some patients complain

about the increased thickness of the secretions. Another disadvantage of the firstgeneration antihistamines is that most must be administered three to four times daily. If first-generation antihistamines are recommended by a health care practitioner, care must be taken to educate the patient about these CNS and anticholinergic side effects. Patients who take other sedative substances are prone to an additive effect from the antihistamine. Those taking any other medications with anticholinergic or antimus-carinic properties may experience additive effects from the antihistamine. The elderly are, in general, more sensitive to both types of adverse effects.

Currently available oral second-generation H1 antihistamines are cetirizine, le-vocetirizine, loratadine, desloratadine, fexofenadine, and acrivastine. All except ac-rivastine are available alone, and some are marketed in combination with the decongestant pseudoephedrine. At the time of this writing, only cetirizine and loratadine are available OTC. The second-generation antihistamines do not have the anticholinergic effects of the first-generation agents. Based on current literature, no single H1 anti-

histamine (first or second generation) is clearly superior in efficacy; however, very few head to head comparative studies have been conducted. The oral second-generation antihistamines are effective for the sneezing, itching, and rhinorrhea of AR, but less effective for the nasal congestion. They also improve ocular symptoms. Intranasal antihistamines are better for nasal congestion.

Fexofenadine has virtually no sedative effects, even at doses higher than usually recommended. Loratadine and desloratadine are not sedative at recommended doses, but can be at higher doses. Cetirizine, levocetirizine, and acrivastine have some sedative effects, even at recommended doses.1 All the oral second-generation agents require some dosage reduction with impaired renal function, although the specific recommendations vary with creatinine clearance.30 To date, none of the currently available oral second-generation antihistamines have been reported to cause QT prolongation or torsade de pointes, as were associated with the two agents that have been removed from the U.S. market (terfenadine and astemizole).13 Most of the oral second-generation antihistamines can be administered once daily (except for the lower dosage forms of fexofenadine), which probably improves adherence.

There are only two intranasal antihistamine products available in the U.S. market at the time of this writing. Both azelastine and olopatadine are considered second-generation agents, although they also have some mast cell stabilizing effects. Both are available only by prescription. The most common side effect of these products is a bitter taste. This occurs in up to 20% of patients on azelastine, and probably somewhat fewer on olopatadine.1 Also, there is enough systemic absorption to cause sedation in some patients using azelastine (about 10%) and perhaps somewhat fewer on olopatadine.1 However, there are no direct comparisons of the two agents, so definitive statements regarding their relative efficacy and side-effect incidence cannot be made. See Table 62-7 for the single-agent second-generation antihistamine products.

© Many patients with mild to moderate AR are adequately treated with an OTC oral first- or (preferably) second-generation antihistamine alone. Others may prefer the intranasal administration of an antihistamine, but these require a prescription. Still others may prefer fexofenadine by prescription due to the absence of sedation. Some patients will need or prefer combination therapy. If nasal congestion is not relieved by the above regimens, addition of a decongestant is reasonable, either alone or as a combination product (see Decongestant section below). Perhaps even the combination of an oral with an intranasal antihistamine is reasonable for some patients, depending on their preferences. Other pharmacologic agents can be combined with oral and/or intranasal antihistamines, as necessary for optimal control of symptoms (see below).

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